Pharmacology - Research Publications
Permanent URI for this collectionhttps://kr.cup.edu.in/handle/32116/111
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Item A focus on Rho/ROCK signaling pathway: An emerging therapeutic target in depression(Elsevier B.V., 2023-03-08T00:00:00) Hanifa, Mohd; Singh, Mohini; Randhawa, Puneet Kaur; Jaggi, Amteshwar Singh; Bali, AnjanaDepression is the most common mental health disorder worldwide; however, the exact cellular and molecular mechanisms of this major depressive disorder are unclear so far. Experimental studies have demonstrated that depression is associated with significant cognitive impairment, dendrite spine loss, and reduction in connectivity among neurons that contribute to symptoms associated with mood disorders. Rho/Rho-associated coiled-coil containing protein kinase (ROCK) receptors are exclusively expressed in the brain and Rho/ROCK signaling has gained considerable attention as it plays a crucial role in the development of neuronal architecture and structural plasticity. Chronic stress-induced activation of the Rho/ROCK signaling pathway promotes neuronal apoptosis and loss of neural processes and synapses. Interestingly, accumulated evidence has identified Rho/ROCK signaling pathways as a putative target for treating neurological disorders. Furthermore, inhibition of the Rho/ROCK signaling pathway has proven to be effective in different models of depression, which signify the potential benefits of clinical Rho/ROCK inhibition. The ROCK inhibitors extensively modulate antidepressant-related pathways which significantly control the synthesis of proteins, and neuron survival and ultimately led to the enhancement of synaptogenesis, connectivity, and improvement in behavior. Therefore, the present review refines the prevailing contribution of this signaling pathway in depression and highlighted preclinical shreds of evidence for employing ROCK inhibitors as disease-modifying targets along with possible underlying mechanisms in stress-associated depression. � 2023 Elsevier B.V.Item Exploring the Potential Role of Nf-Kb Signaling Cascade in Stress Adaptation(Walsh Medical Media, LLC, 2021-12-22T00:00:00) Bali, Anjana; Jaggi, Amteshwar Singh; Bhavya, Aluri SreeThe present study aimed to investigate the role of NF-kB signaling in stress adaptation during exposure of repeated immobilization stress of varying duration in mice. Animals were subjected to two paradigms of immobilization stress i.e., short duration (30 minutes) or long duration (120 minutes). Mice were subjected to homotypic stressor for 5 days to induce stress adaptation. Actophotometer, open field, social interaction and hole board tests were performed to assess stress-associated alteration in behavior; while serum corticosterone levels were measured as a biochemical parameter of stress induction. The levels of p-NF-kB were assessed in stress sensitive prefrontal cortex region. A single episode of short as well as long immobilization stress resulted in changes in behavior, increased plasma corticosterone levels and p-NF-kB levels in prefrontal cortex. In contrast, continuous exposure to short as well as long stress restored behavior, corticosterone and p-NF-kB levels. Treatment with diethyldithiocarbamic acid (DDTC), a selective NF-kB inhibitor, attenuated acute stress associated changes in behavior and corticosterone levels. Moreover, DDTC restored the NF-kB levels in stress subjected mice. It suggests that acute stress may increase the levels of p-NF-kB in the prefrontal cortex may be responsible for the induction of behavioral and biochemical changes. Therefore, NF-kB may serve as an important target in inducing stress adaptation in immobilization stress. Copyright: �2021 Bali A, et al..